Staphylococcus aureus is a facultative anaerobic Gram-positive coccus. It is a microorganism widely distributed in nature and causes both nosocomial and opportunistic infection. It is recognized as a main causative bacterium that induces, for example, food poisoning accompanied by pyelitis, cystitis, impetigo, localized abscess, osteomyelitis, sepsis, and/or vomiting.
In addition, as a type of Staphylococcus aureus, Methicillin-resistant Staphylococcus aureus (MRSA) has been found, which results from chromosomal variation and thus is highly resistant to a variety of antibiotics. MRSA proliferates in persons with compromised immune systems such as elderly persons, newborn infants, and cancer patients so as to cause pneumonia, sepsis, and the like, resulting in death in some cases.
Since MRSA was first reported in England in 1961, MRSA has been known as a bacterium causing nosocomial infection. However, in 1981, an MRSA infection case (community-acquired MRSA), which was not a nosocomial infection case, was reported in the U.S. (see Non-Patent Document 1). Hitherto, many cases of non-nosocomial infections confirmed with MRSA via isolation have been reported all over the world.
Community-acquired MRSA is known to have a bacteriological feature of having a high probability of having a gene encoding PVL that is a leukocytolytic toxin (see Non-Patent Document 2).
The PVL toxin is characterized in that it is a binary toxin comprising two proteins, which are Panton-Valentine leukocidin F (hereinafter referred to as “LukF-PV”) and Panton-Valentine leukocidin S (hereinafter referred to as “LukS-PV”). PVL itself does not have toxic activity; however, it exhibits cytolytic activity specific to leukocytic cells when the two components function in combination.
From 1997 to 1999, deaths from childhood pneumonia/sepsis caused by community-acquired MRSA having the PVL gene were reported in succession in Minnesota and North Dakota in the U.S. (see Non-Patent Document 3). The importance of PVL detection from community-acquired MRSA has been gaining attention. Further, in addition to MRSA, the importance of PVL detection from Staphylococcus aureus has also been gaining attention.
At present, PVL gene detection by the PCR method has been carried out as a PVL detection method (see Non-Patent Documents 4 and 5).
In addition to the above, G. PREVOST et al. produced an antibody against the PVL toxin and they reported an example of immunological detection of the PVL toxin with the use of the antibody (see Non-Patent Document 6).
Further, a method for controlling Staphylococcus aureus with the use of antibiotics or an antibacterial agent has so far been available. However, a method for directly preventing or treating a disorder caused by PVL produced by Staphylococcus aureus has not been established.
Non-Patent Document 1: CDC (Centers for Disease Control) in the U.S.: “Community-acquired methicillin-resistant Staphylococcus aureus infections—Michigan” Morbidity and Mortality Weekly Report, 1981; Vol. 30, pp. 185-187
Non-Patent Document 2: “Community-acquired MRSA gene structure and diagnosis (findings in bacteria)” written by Teruyo Ito et al., The Journal of the Japanese Association for Infectious Diseases, June in 2004, vol. 78, no. 6, pp. 459-469
Non-Patent Document 3: CDC (Centers for Disease Control) in the U.S.: “Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus” Morbidity and Mortality Weekly Report, 1999; Vol. 48, pp. 707-710
Non-Patent Document 4: “Involvement of Panton-Valentine leukocidine-producing Staphylococcus aureus in primary skin infections and pneumonia” written by Lina G, Piemont, Godial-Gamot F. et al., Clinical infectious Diseases, 1999; Vol. 29, pp. 1128-1132
Non-Patent Document 5: “The emergence of Panton-Valentine leukocidin-positive community-acquired Methicillin-resistant Staphylococcus aureus” written by Tatsuo Yamamoto et al., Japanese Journal of Chemotherapy, November in 2004, Vol. 52, pp. 635-653
Non-Patent Document 6: “Characterization of a novel structural member, LukE-LukD, of the bi-component staphylococcal leucotoxins family” written by A. Gravet, G. Prevost et al., FEBS Letters, 1998, Vol. 436, pp. 202-208